Relevant bibliographies by topics / Lung and breast/ovarian cancer

Academic literature on the topic 'Lung and breast/ovarian cancer'

Author: Grafiati
Published: 7 July 2024
Last updated: 7 July 2024

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Journal articles on the topic "Lung and breast/ovarian cancer":

1

Prat, Aleix, Barbara Adamo, Cheng Fan, Maria Vidal, Patricia Galvan, Enriqueta Felip, Jose Maria Del Campo, Josep Tabernero, and Javier Cortes. "Molecular identification of basal-like breast cancer through genomic analyses across five cancer types." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): 1011. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.1011.

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1011 Background: Common molecular alterations in different types of cancer are being identified and these might be successfully targeted regardless of the tumor´s tissue of origin. To better understand the genomic relationships among different types of cancer, we explored global gene expression patterns across breast, lung, ovarian, brain and colorectal cancers. Methods: A unified set of 1,707 samples of 5 human cancer types (breast [n=547], lung [squamous and adenocarcinomas, n=249], ovarian [serous carcinoma, n=489], brain [glioblastoma multiforme, n=202] and colorectal [n=220]) from The Cancer Genome Atlas (TCGA) project was evaluated. All microarrays were performed at the University of North Carolina under the same protocol and platform. All samples provided in each publication of TCGA were used, except for lung adenocarcinomas where we used TCGA public data. Consensus clustering was used to identify molecular entities, and breast cancer intrinsic subtyping was performed using the PAM50 predictor. Results: A total of 6 distinct and robust molecular entities were identified representing tumors from breast luminal/HER2-enriched, breast Basal-like, lung, ovarian, brain and colorectal cancers. Strikingly, 55%, 26%, 16% of Basal-like breast cancers were found to be more similar to squamous cell lung carcinomas, lung adenocarcinomas and ovarian cancers, respectively, compared to breast luminal/HER2-enriched tumors. Breast cancer intrinsic subtyping identified a Basal-like profile in 55% of squamous cell lung cancers, 53% of ovarian cancers and 8% of lung adenocarcinomas. Finally, single genes and gene signatures tracking cancer-related biological processes such as proliferation, angiogenesis and immune activation were found highly expressed in different proportions across the 6 molecular entities. Conclusions: These data suggest that breast tumors of the Basal-like subtype have a distinct cell of origin compared to luminal/HER2-enriched tumors. Clinical trials focusing on tumors with common profiles and/or biomarker expression rather than their tissue of origin are warranted with a special focus on Basal-like breast cancer, squamous cell lung carcinoma and serous ovarian cancer.
2

Achariyapota, Vuthinun, Tuenjai Chuangsuwanich, and Mongkol Benjapibal. "Inflammatory Breast Cancer from Metastatic Ovarian Cancer." Case Reports in Obstetrics and Gynecology 2016 (2016): 1–3. http://dx.doi.org/10.1155/2016/3476143.

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Metastases to the breast from tumors other than breast carcinomas are extremely rare and represent only 0.2–1.3% of all diagnosed malignant breast tumors. Furthermore, while the most common sites for advanced ovarian cancer metastases are the liver, lung, and pleura, metastasis to the breast from a primary ovarian cancer is uncommon and has only been reported in 0.03–0.6% of all breast cancers. Here we describe a case report of a 50-year-old female patient with a rare case of breast metastases from an advanced ovarian cancer, presenting as inflammatory breast cancer. Our observations emphasize the clinical importance of distinguishing between primary and metastatic breast cancer during diagnosis for the purpose of appropriate prognosis and treatment.
3

R., Abhirup H., Priyanka Kenchetty, and Aishwarya K. Chidananda. "Breast ovarian cancer syndrome." International Surgery Journal 8, no. 8 (July 28, 2021): 2454. http://dx.doi.org/10.18203/2349-2902.isj20213144.

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BRCA1 and BRCA2, known as breast and ovarian cancer predisposition genes, were discovered in the 1990s. As part of a normal genetic structure, these genes are intrinsic to all human beings, but they are mutated in some individuals increasing the risk for breast and ovarian cancers development. BRCA1 is not only expressed in endocrine tissues but is also detected in other cells such as the neuroepithelial cells in the early stage of cell development. Like BRCA1, BRCA2 is also expressed in a wide variety of tissues and is observed with higher rates in the breast and thymus and with lower rates in the lung, ovary and spleen. We presented to you a case of 40 year old female admitted in surgical ward with lump in the left breast since 2 months with ipsilateral discrete axillary lymphadenopathy. Bilateral sono-mammography showed BIRADS V lesion in left breasts with satellite nodules. Ultrasonography of abdomen and pelvis showed large left adnexal solid mass lesion and right sided ovarian cyst with retrocaval, preaortic lymphadenopathy. Patient underwent a diagnostic laparoscopy which was converted to a laparotomy. Total abdominal hysterectomy with bilateral salphingo-oophorectomy was done. For the breast lump, patient underwent left sided modified radical mastectomy. Gene testing for revealed BRCA1 positivity. Chemotherapy was given to cover both breast and ovarian carcinoma. Patient came back with abdominal distension after 9 months and was offered palliative care. Patient succumbed for disease after 1 year after diagnosis. We reviewed the literature for the same.
4

Abu-Tineh, Mohammad, Hind Elmalik, and Mohamed A. Yassin. "Metastatic Ovarian Cancer Presenting as Inflammatory Breast Cancer: A Case Report." Case Reports in Oncology 13, no. 2 (July 28, 2020): 867–74. http://dx.doi.org/10.1159/000508358.

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Metastatic ovarian cancer to the breast is a rare presentation, with limited cases reported worldwide. Common sites for distant metastasis in ovarian cancer are to the liver, lung, and pleura [Dauplat et al. Cancer. 1987 Oct 1;60(7):1561–6]. Usually, such cases predict poor prognosis with troublesome management. We present one challenging case of a 54-year-old female patient with recurrent clear cell ovarian cancer, presenting with right breast mass of primary versus secondary origin, progressing into inflammatory breast cancer picture. Our report aims to shed light on the value of early suspicion and low threshold of detecting secondary breast masses of ovarian cancer origin.
5

Bacalbasa, Nicolae, Irina Balescu, Claudia Stoica, Cristina Martac, Valentin Varlas, Andrei Voichitoiu, Lucian Pop, Sorin Petrea, Mihaela Vilcu, and Iulian Brezean. "Breast metastases from ovarian cancer." Romanian Medical Journal 69, S4 (June 20, 2022): 14–16. http://dx.doi.org/10.37897/rmj.2022.s4.3.

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Ovarian cancer represents one of the most aggressive malignancies which is characterized by a high capacity of spread via multiple pathways such as lymphatic, peritoneal and hematogenous route, the most commonly encountered sites for metastatic lesions being represented by lung, liver, peritoneum and lymph nodes. In extremely rare cases breast metastases with ovarian origin have been reported. In such cases different therapeutic strategies have been proposed; however the overall prognosis remains extremely poor, the presence of metastatic lesions at this level being usually the sign of disseminated disease.
6

Arora, Nimisha, Aline Talhouk, Jessica N. McAlpine, Michael R. Law, and Gillian E. Hanley. "Causes of death among women with epithelial ovarian cancer by length of survival post-diagnosis: a population-based study in British Columbia, Canada." International Journal of Gynecologic Cancer 29, no. 3 (December 21, 2018): 593–98. http://dx.doi.org/10.1136/ijgc-2018-000040.

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ObjectivesLittle is known regarding the health of women who survive more than 5 years following their ovarian cancer diagnosis. To bridge an important gap in our knowledge about long term health of ovarian cancer survivors, we examined the causes of death among women diagnosed with epithelial ovarian cancer between 1990 and 2014 in British Columbia. These causes were stratified by years since diagnosis, and compared with age- standardized causes of death among women who have not been diagnosed with ovarian cancer.MethodsWe examined all women with epithelial ovarian cancer in British Columbia 1990–2014 using population- based administrative datasets. We stratified women into three groups: all epithelial ovarian cancer patients; women surviving 5 to 9 years post-diagnosis, and women surviving 10 or more years since diagnosis. All- cause and cause specific standardized mortality ratios (SMRs) were calculated.ResultsThere were 4246 deaths among 6427 women with epithelial ovarian cancer. About 55.9% of deaths were from ovarian cancer. When compared with the general population, the highest SMRs (SMR of 5 or higher) were for deaths from other cancers and external causes (44.4% from falls) among women surviving 5–9 years and 10 or more years post-diagnosis. Mortality from other cancers can largely be explained by deaths from breast cancer (15.8%), lung cancer (12.3%), and colorectal cancer (11%).ConclusionsWhile the majority of epithelial ovarian cancer patients continue to die from their ovarian cancer, our results suggest that long term ovarian cancer survivors are particularly vulnerable to deaths from other cancers and from falls in elderly survivors. These data could indicate closer surveillance for breast, lung, and colorectal cancer, and closer attention to bone health is warranted among women surviving for 5 or more years following their epithelial ovarian cancer diagnosis.
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Haan, David, Anna Bergamaschi, Yuhong Ning, William Gibb, Michael Kesling, Adriana Pitea, Maryam Nabiyouni, et al. "Genome-wide 5hmC profiles to enable cancer detection and tissue of origin classification in breast, colorectal, lung, ovarian, and pancreatic cancers." Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021): 3044. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.3044.

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3044 Background: Epigenomics assays have recently become popular tools for identification of molecular biomarkers, both in tissue and in plasma. In particular 5-hydroxymethyl-cytosine (5hmC) method, has been shown to enable the epigenomic regulation of gene expression and subsequent gene activity, with different patterns, across several tumor and normal tissues types. In this study we show that 5hmC profiles enable discrete classification of tumor and normal tissue for breast, colorectal, lung ovary and pancreas. Such classification was also recapitulated in cfDNA from patient with breast, colorectal, lung, ovarian and pancreatic cancers. Methods: DNA was isolated from 176 fresh frozen tissues from breast, colorectal, lung, ovary and pancreas (44 per tumor per tissue type and up to 11 tumor tissues for each stage (I-IV)) and up to 10 normal tissues per tissue type. cfDNA was isolated from plasma from 783 non-cancer individuals and 569 cancer patients. Plasma-isolated cfDNA and tumor genomic DNA, were enriched for the 5hmC fraction using chemical labelling, sequenced, and aligned to a reference genome to construct features sets of 5hmC patterns. Results: 5hmC multinomial logistic regression analysis was employed across tumor and normal tissues and identified a set of specific and discrete tumor and normal tissue gene-based features. This indicates that we can classify samples regardless of source, with a high degree of accuracy, based on tissue of origin and also distinguish between normal and tumor status.Next, we employed a stacked ensemble machine learning algorithm combining multiple logistic regression models across diverse feature sets to the cfDNA dataset composed of 783 non cancers and 569 cancers comprising 67 breast, 118 colorectal, 210 Lung, 71 ovarian and 100 pancreatic cancers. We identified a genomic signature that enable the classification of non-cancer versus cancers with an outer fold cross validation sensitivity of 49% (CI 45%-53%) at 99% specificity. Further, individual cancer outer fold cross validation sensitivity at 99% specificity, was measured as follows: breast 30% (CI 119% -42%); colorectal 41% (CI 32%-50%); lung 49% (CI 42%-56%); ovarian 72% (CI 60-82%); pancreatic 56% (CI 46%-66%). Conclusions: This study demonstrates that 5hmC profiles can distinguish cancer and normal tissues based on their origin. Further, 5hmC changes in cfDNA enables detection of the several cancer types: breast, colorectal, lung, ovarian and pancreatic cancers. Our technology provides a non-invasive tool for cancer detection with low risk sample collection enabling improved compliance than current screening methods. Among other utilities, we believe our technology could be applied to asymptomatic high-risk individuals thus enabling enrichment for those subjects that most need a diagnostic imaging follow up.
8

Tkaczuk, Katherine R., Paula Rosenblatt, Ranee Mehra, Katherine A. Scilla, Nancy Tait, Katerra Caple, Binbin Yue, and Ginette Serrero. "Abstract CT240: On-going phase 1A clinical trial for AG01 an first-in-class anti-progranulin (GP88) monoclonal antibody in patients with advanced malignancies." Cancer Research 83, no. 8_Supplement (April 14, 2023): CT240. http://dx.doi.org/10.1158/1538-7445.am2023-ct240.

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Abstract Progranulin (PGRN/GP88) is an 88 kDa glycoprotein characterized by seven and a half double cysteine rich repeats which is the largest member of the granulin-epithelin protein family. PGRN/GP88 has been demonstrated as a biological driver of tumorigenesis, survival, and drug resistance in several cancers including breast cancer (BC), lung prostate, ovarian and digestive cancers. PGRN/GP88 tissue expression is an independent prognostic factor of recurrence in breast, lung cancers while elevated serum PGRN/GP88 level in metastatic breast, lung, ovarian and prostate cancer patients. Elevated PGRN/GP88 levels are associated with poor outcomes such as progression and shortened survival. An anti-human PGRN/GP88 monoclonal antibody able to inhibit PGRN/GP88 action in vitro and in vivo has been developed, chimerized and expressed in CHO cells. All IND enabling activities including pharmacology, GMP manufacturing, formulation and GLP toxicology studies have been conducted. The IND application has been filed and cleared by the Food and Drug Administration. A first-in-human, first-in-class phase 1 safety and efficacy clinical study of AG01 in patients with solid tumors and advanced disease with special focus on patients with breast, lung and ovarian cancers has been initiated and is on-going at the University of Maryland Greenebaum Cancer Center. The trial is registered as NCT05627960 to clinicaltrials.gov site. Supported by grants R44CA162629 and R44CA224718 from the National Cancer Institute to GS. Citation Format: Katherine R. Tkaczuk, Paula Rosenblatt, Ranee Mehra, Katherine A. Scilla, Nancy Tait, Katerra Caple, Binbin Yue, Ginette Serrero. On-going phase 1A clinical trial for AG01 an first-in-class anti-progranulin (GP88) monoclonal antibody in patients with advanced malignancies [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 2 (Clinical Trials and Late-Breaking Research); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(8_Suppl):Abstract nr CT240.
9

Roland, Adjoby Cassou, Kouamé Arthur Didier, Koffi Achille, Kakou Charles, Konan Joachim, Andriamandimbison Zoly, Ahounkeng Patrick, and Nshimirimana Eric. "Metastatic ovarian tumor of a lung cancer at the hospital center of Chauny (France): a case report." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 6, no. 10 (September 23, 2017): 4682. http://dx.doi.org/10.18203/2320-1770.ijrcog20174464.

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The ovary is an organ that can be the site of metastases for many cancers. In general, malignant ovarian tumors are primary; however, cases of extra gynecological metastatic tumors (breast, colon, stomach, and pancreas) have been reported. In most cases, the primary cancers of these ovarian tumors are gastrointestinal or gynecological, the lung being very rarely involved. We report a rare case of ovarian metastases of bronchial cancer discovered during an extensional assessment. The histological examination coupled with immunohistochemistry concludes that ovarian metastasis of small cell lung carcinoma. In addition to chemotherapy such as Taxol-Hycamtin, the management required cerebral radiotherapy for a cerebral metastasis detected.
10

Yurkovetsky, Zoya, Steven Skates, Aleksey Lomakin, Brian Nolen, Trenton Pulsipher, Francesmary Modugno, Jeffrey Marks, et al. "Development of a Multimarker Assay for Early Detection of Ovarian Cancer." Journal of Clinical Oncology 28, no. 13 (May 1, 2010): 2159–66. http://dx.doi.org/10.1200/jco.2008.19.2484.

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PurposeEarly detection of ovarian cancer has great promise to improve clinical outcome.Patients and MethodsNinety-six serum biomarkers were analyzed in sera from healthy women and from patients with ovarian cancer, benign pelvic tumors, and breast, colorectal, and lung cancers, using multiplex xMAP bead-based immunoassays. A Metropolis algorithm with Monte Carlo simulation (MMC) was used for analysis of the data.ResultsA training set, including sera from 139 patients with early-stage ovarian cancer, 149 patients with late-stage ovarian cancer, and 1,102 healthy women, was analyzed with MMC algorithm and cross validation to identify an optimal biomarker panel discriminating early-stage cancer from healthy controls. The four-biomarker panel providing the highest diagnostic power of 86% sensitivity (SN) for early-stage and 93% SN for late-stage ovarian cancer at 98% specificity (SP) was comprised of CA-125, HE4, CEA, and VCAM-1. This model was applied to an independent blinded validation set consisting of sera from 44 patients with early-stage ovarian cancer, 124 patients with late-stage ovarian cancer, and 929 healthy women, providing unbiased estimates of 86% SN for stage I and II and 95% SN for stage III and IV disease at 98% SP. This panel was selective for ovarian cancer showing SN of 33% for benign pelvic disease, SN of 6% for breast cancer, SN of 0% for colorectal cancer, and SN of 36% for lung cancer.ConclusionA panel of CA-125, HE4, CEA, and VCAM-1, after additional validation, could serve as an initial stage in a screening strategy for epithelial ovarian cancer.
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Journal articles Dissertations / Theses Books

Dissertations / Theses on the topic "Lung and breast/ovarian cancer":

1

Woods, Tonya M. "Extracting meaningful statistics for the characterization and classification of biological, medical, and financial data." Diss., Georgia Institute of Technology, 2015. http://hdl.handle.net/1853/53857.

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This thesis is focused on extracting meaningful statistics for the characterization and classification of biological, medical, and financial data and contains four chapters. The first chapter contains theoretical background on scaling and wavelets, which supports the work in chapters two and three. In the second chapter, we outline a methodology for representing sequences of DNA nucleotides as numeric matrices in order to analytically investigate important structural characteristics of DNA. This methodology involves assigning unit vectors to nucleotides, placing the vectors into columns of a matrix, and accumulating across the rows of this matrix. Transcribing the DNA in this way allows us to compute the 2-D wavelet transformation and assess regularity characteristics of the sequence via the slope of the wavelet spectra. In addition to computing a global slope measure for a sequence, we can apply our methodology for overlapping sections of nucleotides to obtain an evolutionary slope. In the third chapter, we describe various ways wavelet-based scaling may be used for cancer diagnostics. There were nearly half of a million new cases of ovarian, breast, and lung cancer in the United States last year. Breast and lung cancer have highest prevalence, while ovarian cancer has the lowest survival rate of the three. Early detection is critical for all of these diseases, but substantial obstacles to early detection exist in each case. In this work, we use wavelet-based scaling on metabolic data and radiography images in order to produce meaningful features to be used in classifying cases and controls. Computer-aided detection (CAD) algorithms for detecting lung and breast cancer often focus on select features in an image and make a priori assumptions about the nature of a nodule or a mass. In contrast, our approach to analyzing breast and lung images captures information contained in the background tissue of images as well as information about specific features and makes no such a priori assumptions. In the fourth chapter, we investigate the value of social media data in building commercial default and activity credit models. We use random forest modeling, which has been shown in many instances to achieve better predictive accuracy than logistic regression in modeling credit data. This result is of interest, as some entities are beginning to build credit scores based on this type of publicly available online data alone. Our work has shown that the addition of social media data does not provide any improvement in model accuracy over the bureau only models. However, the social media data on its own does have some limited predictive power.
2

Ducrot, Lucas. "Réseaux bayésiens et analyse de survie pour l’estimation de courbes de pénétrance du cancer broncho-pulmonaire lié à des prédispositions génétiques." Electronic Thesis or Diss., Sorbonne université, 2024. http://www.theses.fr/2024SORUS055.

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Cette thèse se concentre sur l'estimation de courbes de pénétrance de maladies génétiques à partir de données de pédigrée, avec un intérêt particulier pour la prédisposition génétique au cancer broncho-pulmonaire. Dans ce contexte, elle vise à proposer des résultats à la fois cliniques et épidémiologiques ainsi que des résultats méthodologiques.Les consultations en génétique sont proposées aux patients ayant des antécédents familiaux sévères de maladies génétiques. Les médecins généticiens doivent sélectionner, parmi ces patients, lesquels se voient proposer un test génétique, ainsi qu'évaluer les risques de maladie pour ces patients et leurs familles. La progression des connaissances en génétique est rapide et le nombre de variants pathogènes identifiés pour différentes maladies augmentent chaque année. Cela entraine un besoin d'outils de prédiction et d'évaluation de risque important, en particulier dans le cadre du cancer broncho-pulmonaire. En effet, les liens entre ce dernier et des variants pathogènes (SFTPA1/SFTPA2 et sur les gènes TP53 et EGFR) sont connus mais encore peu décrits.Les méthodes existantes pour évaluer le risque de survenue de maladies reposent sur les courbes de pénétrance, mais leur estimation présente des défis en raison du faible nombre de patients et du biais de sélection omniprésent dans les jeux de données collectés en génétique. Pour surmonter ces obstacles, la thèse explore l'utilisation de données familiales, en utilisant un ensemble d'outils statistiques dont les réseaux bayésiens, les modèles de mélange et l'analyse de survie, ainsi que des modèles existants, pour lesquels elle tente d'affaiblir certaines hypothèses.Le chapitre 1 propose une présentation du contexte médical de la thèse, introduisant les notions de maladies génétiques et de conseil en génétique. Le chapitre 2 est une introduction méthodologique présentant, et illustrant sur des exemples, les concepts d'analyse de survie, de réseaux bayésiens, d'algorithme somme-produit, de modèles de mélanges et d'algorithme EM. Il propose également un état de l'art de l'estimation de courbe de pénétrance pour des maladies génétiques et une mise en évidence du biais de sélection en génétiques. Il se conclue par un récapitulatif des questions de recherche abordées.Cette thèse s'est, ensuite, orientée autour de quatre projets. Les deux premiers projets, correspondant aux chapitres 3 et 4, proposent des résultats plutôt cliniques et épidémiologiques. La premier projet, décrit au chapitre 3, porte sur une comparaison de différentes méthodes de prédiction de variants pathogènes pour les cancers sein/ovaire (Score de Manchester et modèles familiaux, type BOADICEA). Le second projet, abordé au chapitre 4, propose une estimation des pénétrances de la pneumopathie interstitielle et du cancer broncho-pulmonaire pour les porteurs de variants pathogènes SFTPA1 et SFTPA2.Les deux derniers projets, correspondant aux chapitres 5 et 6, sont plus méthodologiques. Le chapitre 5 est consacré au développement d'une nouvelle méthode d'estimation de courbe de pénétrance de maladie génétique à partir de données de pédigrée lorsque la maladie présente des cas sporadiques. Elle se base sur une contrainte d'incidence de la maladie en population générale et une paramétrisation du ratio de risques instantanés entre les porteurs et les non-porteurs de variants pathogènes. Le chapitre 6 se consacre, lui, à la mise en évidence du biais introduit par la sélection en génétique et ses conséquences sur les résultats de la méthode développée au chapitre 5. Des méthodes de corrections connues, comme la Proband's phenotype Exclusion Likelihood (PEL) et la Genotype-Restricted Likelihood (GRL), combinées à notre méthode, sont appliquées à des données simulées
This thesis focuses on estimating penetrance curves of genetic diseases from pedigree data, with a particular interest in the genetic predisposition to bronchopulmonary cancer. In this context, it aims to provide clinical and epidemiological results, as well as methodological findings.Genetic counselling is offered to patients with severe family histories of genetic diseases. Geneticists must select from these patients who should be offered genetic testing, and assess the disease risks for these patients and their families. Advances in genetics are rapid, and the number of identified pathogenic variants for different diseases increases each year. This necessitates significant predictive and risk assessment tools, especially in the context of bronchopulmonary cancer. Indeed , the links between the latter and pathogenic variants (such that SFTPA1/SFTPA2 and the genes TP53 and EGFR) are known but still poorly described.Existing methods for assessing the risk of disease occurrence rely on penetrance curves, but their estimation faces challenges due to the small number of patients and the omnipresent selection bias in genetics-collected datasets. To overcome these obstacles, the thesis explores the use of familial data, employing a set of statistical tools including Bayesian networks, mixture models, survival analysis, as well as existing models, for which it attempts to weaken certain assumptions.Chapter 1 provides an overview of the medical context of the thesis, introducing the concepts of genetic diseases and genetic counseling. Chapter 2 serves as a methodological introduction, presenting and illustrating concepts such as survival analysis, Bayesian networks, sum-product algorithm, mixture models and EM algorithm, using examples. It also offers a state-of-the-art review of penetrance curve estimation for genetic diseases and highlights the selection bias in genetics. The chapter concludes with a summary of the addressed research questions.Then, the thesis revolves around four projects. The first two projects, corresponding to chapters 3 and 4, offer predominantly clinical and epidemiological results. The first project, described in Chapter 3, compares different methods for predicting pathogenic variants for breast/ovarian cancers (Manchester Score and family models like BOADICEA). The second project, addressed in Chapter 4, provides estimates of penetrance for interstitial lung disease and bronchopulmonary cancer for carriers of pathogenic variants SFTPA1 and SFTPA2.The last two projects, corresponding to chapters 5 and 6, are more methodological. Chapter 5 is dedicated to developing a new method for estimating the penetrance curve of a genetic disease from pedigree data when the disease presents sporadic cases. It is based on an incidence constraint of the disease in the general population and a parameterization of the relative hazard between carriers and non-carriers of pathogenic variants. Chapter 6 focuses on highlighting the bias introduced by selection in genetics and its consequences on the results of the method developed in Chapter 5. Known correction methods, such as Proband's Phenotype Exclusion Likelihood (PEL) and Genotype-Restricted Likelihood (GRL), combined with our method, are applied to simulated data
3

Vehmanen, Paula. "Breast cancer-predisposing genes in Finnish breast and ovarian cancer families." Helsinki : University of Helsinki, 2001. http://ethesis.helsinki.fi/julkaisut/mat/bioti/vk/vehmanen/.

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4

Ford, Deborah. "Genetic epidemiology of breast and ovarian cancer." Thesis, Institute of Cancer Research (University Of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367527.

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Schofield, Andrew C. "Molecular genetics of breast and ovarian cancer." Thesis, University of Aberdeen, 1998. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU100481.

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Breast cancer is one of the most common malignancies in women, affecting one in twelve. Ovarian cancer, although not as frequent, is the leading cause of death from gynaecological cancer. Inherited predisposition to breast and ovarian cancer, which accounts for approximately 5 to 10% of these cancers, has been associated with mutations in the BRCA1 and BRCA2 genes. Mutations in both of these genes increase the lifetime risk of developing breast cancer by approximately 80%. BRCA1 confers a greater predisposition of ovarian cancer than BRCA2, however, BRCA2 has been associated with male breast cancer. Polymorphisms linked to BRCA1 and BRCA2 were studied to examine whether either of these genes were linked to breast and breast/ovarian cancer families. None of the five cancer families studied generated statistically significant lod scores although the segregation of a common haplotype with the disease in each family and positive lod scores did suggest that four of these families were linked to BRCA1 and the other to BRCA2. Subsequent mutation studies identified three germline mutations, thus confirming the initial linkage results in three families. A total of four deletions and six polymorphisms were identified in BRCA1 and BRCA2 from forty-eight breast and breast/ovarian cancer families, using SSCP analysis and PTT. The functional effect of these mutations is unclear although variable expression of the cancer phenotype suggests that other genes and environmental factors play an important role in the development of breast and ovarian cancer. Evidence of an abnormal protein was detected by the presence of clonal LOH of the normal allele, using BRCA1 antibodies in familial breast and ovarian tumours. In addition, BRCA1 immunostaining was negative in a greater proportion of benign tumours compared to malignant ovarian tumours. The loss of BRCA1 does not lead to malignancy, suggesting that BRCA1 may have another role in benign ovarian epithelial tumours.
6

Huusko, P. (Pia). "Predisposing genes in hereditary breast and ovarian cancer." Doctoral thesis, University of Oulu, 1999. http://urn.fi/urn:isbn:9514254422.

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Abstract In the present study, mutations in BRCA1 and BRCA2, the two major genes predisposing individuals to hereditary breast and ovarian cancer, were screened in Finnish and Turkish cancer families. Germline BRCA1 mutations were found in 7% (6/88) and BRCA2 mutations in 6% (5/88) of the Finnish families studied in Oulu. Two distinct BRCA1 (3745delT, 4216nt-2A→G) and three BRCA2 (999delTCAAA, 6503delTT, 9346nt-2A→G) mutations were identified, all of which are recurrently found in Finland. In the 15 Turkish cancer families studied, 5382insC and 5622C→T were detected in BRCA1, and 3414delTCAG in BRCA2. The novel 3414del4 mutation was found in a family with a case of male breast cancer. In order to determine their ages and origin, 9 recurrent Finnish BRCA1 and BRCA2 mutations were studied further as regards haplotype conservation. Common origins approximately 18–80 generations (400–1600 years) ago were demonstrated for all studied mutations by partial haplotype sharing. The majority of the mutations showed geographical clustering, supporting the theory of regional founder effects. Four of the nine mutations are unique for Finland, whereas five have also been seen elsewhere. Mutations in the 5' end of BRCA1 tend to predispose individuals to ovarian cancer and those found in the 3' end to breast cancer. The age of ovarian cancer onset was significantly lower for BRCA1 (51 years) than for BRCA2 mutation carriers (61 years). Germline TP53 mutations were sought in the Finnish breast cancer families found to be negative after BRCA1 and BRCA2 screening but who exhibited some phenotypic features of the Li-Fraumeni syndrome. The Asn235Ser was found in a family displaying Li-Fraumeni syndrome phenotype and the Tyr220Cys in a family with a milder Li-Fraumeni-like phenotype. The nature of both mutations as cancer-predisposing alterations was supported by means of loss of heterozygosity (LOH) and p53 immunohistochemistry studies. Regional clustering of BRCA1 and BRCA2 founder mutations enables targeted genetic tests including especially those mutations characteristic of the birthplace of each patient. Additional genes are likely to explain a large proportion of the inherited susceptibility to breast cancer in particular. Germline TP53 mutations are expected to be found in the breast cancer families with other clinical features seen in the Li-Fraumeni syndrome.
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Xintaropoulou, Chrysi. "Targeting aerobic glycolysis in breast and ovarian cancer." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/29525.

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Cancer cells, unlike normal tissue, frequently rely on glycolysis for the production of energy and the metabolic intermediates required for their growth regardless of cellular oxygenation levels. This metabolic reconfiguration, termed the Warburg effect, provides a potential strategy to preferentially target tumours from a therapeutic perspective. The present study sought to investigate the glycolytic phenotype of breast and ovarian cancer, and assess the possibility of exploiting several glycolytic targets therapeutically. Initially the growth dependency of breast and ovarian cancer cells on the availability of glucose was established. An array of 10 compounds reported to inhibit key enzymes of the glycolytic pathway were investigated and compared against an extended panel of breast and ovarian cancer cell line models. All inhibitors investigated, targeted against multiple points of the pathway, were shown to block the glycolytic pathway as demonstrated by glucose accumulation in the culture media combined with decreased lactate secretion, and attenuated breast and ovarian cancer cell proliferation in a concentration dependent manner. Furthermore their mechanism of action was investigated by flow cytometric analysis and their antiproliferative effect was associated with induction of apoptosis and G0/G1 cell cycle arrest. The glycolytic inhibitors were further assessed in combination strategies with established chemotherapeutic and targeted agents and several synergistic interactions, characterised by low combination index values, were revealed. Among them, 3PO (a novel PFKFB3 inhibitor) enhanced the effect of cisplatin in both platinum sensitive and platinum resistant ovarian cancer cells suggesting a strategy for treatment of platinum resistant disease. Furthermore robust synergy was identified between IOM-1190 (a novel GLUT1 inhibitor) and metformin, an antidiabetic inhibitor of oxidative phosphorylation, resulting in strong inhibition of breast cancer cell growth. This combination is proposed for the treatment of highly aggressive triple negative breast tumours. An additional objective of this research was to investigate the effect of the oxygen level on sensitivity to glycolysis inhibition. Breast cancer cells were found to be more sensitive to glycolysis inhibition in high oxygen conditions. This enhanced resistance at low oxygen levels was associated with upregulation of the targeted glycolytic enzymes as demonstrated at both the mRNA (by gene expression microarray profiling, Illumina BeadArrays) and protein level (by Western blotting). Manipulation of LDHA (Lactate Dehydrogenase A) by siRNA knockdown provided further evidence that downregulation of this target was sufficient to significantly suppress breast cancer cell proliferation. Finally, the expression of selected glycolytic targets was examined in a clinical tissue microarray set of a large cohort of ovarian tumours using quantitative immunofluorescence technology, AQUA. The role of the glycolytic phenotype in ovarian cancer was suggested and interesting associations between the glycolytic profile and clear cell and endometrioid ovarian cancers revealed. Increased PKM2 (Pyruvate kinase isozyme M2) and LDHA expression were demonstrated in clear cell tumours and also low expression of these enzymes was significantly correlated with improved survival of endometrioid ovarian cancer patients. Taken together the findings of this study support the glycolytic pathway as a legitimate target for further investigation in breast and ovarian cancer treatment.
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Cheng, Wing-ming Edward. "Emotional well-being in Chinese lung cancer patients." Click to view the E-thesis via HKUTO, 2004. http://sunzi.lib.hku.hk/hkuto/record/B3197157X.

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Harbord, Sara Helen Alison. "X chromosome studies and breast and ovarian carcinoma." Thesis, University of British Columbia, 2007. http://hdl.handle.net/2429/212.

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Skewed somatic X inactivation (XCI), X-linked gene overexpression and abnormal X content have been associated with breast and ovarian cancer. Partial or complete reactivation of the inactive X in females may be a step in breast and ovarian cancer progression, leading to overexpression of some tumour enhancing gene. Markers of an X reactivation event were examined: X gene dosage, expression, and methylation in 8 ovarian cancer cell lines. Another marker of an X reactivation event, skewed XCI, was assayed in peripheral blood DNA from 106 breast and/or ovarian cancer patients (52 BRCA1 mutation carriers, 24 BRCA2 mutation carriers, 30 non-mutation carriers), 147 age-matched population controls. Combined RNA/DNA FISH was used to quantify the number of inactive Xs compared to total number of Xs. Five cell lines had increased X content. Three cell lines localized XIST to the presumptive inactive X; however the numbers of inactive Xs were variable. Expression levels of 8 X-linked genes were assessed by real-time PCR. Expression was inconsistent between different genes and among cell lines, ranging from a 2 to 300-fold increase compared to a control. Overall, expression was greatly increased for genes subject to inactivation but not increased in genes that escape inactivation for most ovarian cancer cell lines. Methylation at AR and FMR1 was quantified by a real-time PCR based assay and SNuPE respectively. Methylation was lower than expected for 7 of 8 ovarian cancer cell lines at AR or FMR1, while three cell lines had low or no methylation for both genes. Skewed XCI was evaluated using a methylation-based PCR assay at AR. There was no significant increase in skewing above 90% for any cancer group assayed. In addition, two markers of X reactivation were assayed in two low passage cultures of normal ovarian surface epithelium from BRCA1 mutation positive breast cancer patients. One sample did not localize XIST to the inactive X and three of five genes subject to inactivation were overexpressed. In summary, there is evidence for loss of X silencing or gain of active X content in ovarian cancer cell lines and normal ovarian surface epithelium from BRCA1 mutation carriers.
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Bendrik, Christina. "Angiogenesis regulation in hormone dependent breast- and ovarian cancer." Doctoral thesis, Linköpings universitet, Institutionen för klinisk och experimentell medicin, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-63745.

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Angiogenesis is a key event in tumor progression and a rate-limiting step in the establishment of a clinical cancer disease. The net balance of pro- and anti-angiogenesis mediators in the tissue dictates the angiogenic phenotype of a tumor. Matrix metalloproteinases (MMPs) are major regulators of extracellular matrix turnover and have for long been associated with pro-tumorigenic activities due to their tissue degradation capacities. However, broad-spectra MMP inhibitors as anti-tumor therapy in clinical trials have failed, and it has now become evident that several MMPs may induce biological activities beneficial to the host, such as suppressed angiogenesis. In this thesis the protective role of specific MMPs in breast and ovarian tumor tissues was further demonstrated. The process of angiogenesis is essential for physiological functions in the female reproductive tract, where sex steroids regulate new blood vessel formation and regression in each cycle. Despite progress made during the past years, our knowledge in sex steroid regulation of angiogenesis in hormone-dependent tumor tissues remains limited. Tamoxifen is a cornerstone in the treatment of estrogen receptor (ER)-positive breast cancer. The therapeutic value of tamoxifen in the treatment of ER-positive ovarian cancer is to date less investigated. The results presented in this thesis suggest that tamoxifen may induce anti-tumorigenic responses in ER-positive ovarian cancer by means of both anti-proliferative and anti-angiogenic mechanisms. In experimental models of human ovarian cancer in vitro and in vivo, tamoxifen treatment increased extracellular levels of MMP-9 and enhanced generation of the angiogenesis inhibitor endostatin which resulted in significantly decreased angiogenesis and tumor growth. Low levels of MMP-9 and endostatin in ascites collected from ovarian cancer patients suggest a possibility to therapeutically enhance MMP-9 by administration of tamoxifen, and thereby counteract angiogenesis in ovarian tumors by increased generation of anti-angiogenesis fragments, such as endostatin. The significance of enhanced MMP activities in tumor tissues was further investigated by experimental models of intratumoral MMP gene transfer to human breast tumor xenografts, which were assessed by using microdialysis. Treatment of tumors with MMP-9 or MMP-3 resulted in dose-dependent inhibition of tumor growth. Low dose of either MMP induced tumor stasis whereas a higher dose induced significant tumor regression. MMP-9 and tamoxifen exerted synergistic therapeutic effects on breast tumor angiogenesis and growth whereas gene transfer of the MMP-inhibitor TIMP-1 counteracted the beneficial effects induced by tamoxifen. Further on, we confirm the pro-angiogenic potential of estradiol by demonstrating a significant correlation between local levels of estradiol and the pro-angiogenic cytokine IL-8 in normal human breast tissues and in ER/PgR-positive breast cancers of women. Estradiol-induced IL-8 secretion was additionally confirmed in normal human whole breast biopsies in culture and in experimental human breast cancer in vitro and in vivo. In conclusion, the results of this thesis may hopefully increase the overall understanding of several mechanisms involved in angiogenesis regulation and may additionally be useful in the development of novel approaches for targeted therapy in the treatment of hormone-sensitive breast- and ovarian cancer.
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Books on the topic "Lung and breast/ovarian cancer":

1

Bellenir, Karen. Cancer sourcebook for women: Basic consumer health information about gynecologic cancers and other cancers of special concern to women, including cancers of the breast, cervix, colon, lung, ovaries, thyroid, and uterus; along with facts about benign conditions of the female reproductive system, cancer risk factors, screening and prevention programs, women's issues in cancer treatment ... 4th ed. Detroit, MI: Omnigraphics, 2010.

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Nakamura, Seigo, Daisuke Aoki, and Yoshio Miki, eds. Hereditary Breast and Ovarian Cancer. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-4521-1.

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Kemeny, M. Margaret. Breast cancer and ovarian cancer: Beating the odds. Reading, Mass: Addison-Wesley, 1992.

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Aoki, Daisuke, Seigo Nakamura, and Yoshio Miki, eds. Practical Guide to Hereditary Breast and Ovarian Cancer. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-99-5231-1.

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1963-, Morrison Patrick J., Hodgson S. V, and Haites Neva E. 1947-, eds. Familial breast and ovarian cancer: Genetics, screening, and management. Cambridge, UK: Cambridge University Press, 2002.

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1963-, Morrison Patrick J., Hodgson S. V, and Haites Neva E. 1947-, eds. Familial breast and ovarian cancer: Genetics, screening, and management. Cambridge: Cambridge University Press, 2005.

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1940-, Hayat M. A., ed. Lung and breast carcinomas. Amsterdam: Elsevier, Academic Press, 2008.

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Lange, Vladimir. Be a survivor: Lung cancer treatment guide. 2nd ed. Los Angeles, CA: Lange Productions, 2012.

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Hartikainen, Jaana. Genetic predispossition to breast and ovarian cancer in Eastern Finnish population. Kuopio: University of Kuopio, 2007.

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National Cancer Institute (U.S.). Genetic testing for breast and ovarian cancer risk: It's your choice. 2nd ed. Bethesda, Md.]: U.S. Dept. of Health and Human Services, National Institutes of Health, National Cancer Institute, 2005.

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Book chapters on the topic "Lung and breast/ovarian cancer":

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Workman, Paul. "Reflections and Outlook on Targeting HSP90, HSP70 and HSF1 in Cancer: A Personal Perspective." In Advances in Experimental Medicine and Biology, 163–79. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-40204-4_11.

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Abstract This personal perspective focuses on small-molecule inhibitors of proteostasis networks in cancer—specifically the discovery and development of chemical probes and drugs acting on the molecular chaperones HSP90 and HSP70, and on the HSF1 stress pathway. Emphasis is on progress made and lessons learned and a future outlook is provided. Highly potent, selective HSP90 inhibitors have proved invaluable in exploring the role of this molecular chaperone family in biology and disease pathology. Clinical activity was observed, especially in non small cell lung cancer and HER2 positive breast cancer. Optimal use of HSP90 inhibitors in oncology will likely require development of creative combination strategies. HSP70 family members have proved technically harder to drug. However, recent progress has been made towards useful chemical tool compounds and these may signpost future clinical drug candidates. The HSF1 stress pathway is strongly validated as a target for cancer therapy. HSF1 itself is a ligandless transcription factor that is extremely challenging to drug directly. HSF1 pathway inhibitors have been identified mostly by phenotypic screening, including a series of bisamides from which a clinical candidate has been identified for treatment of ovarian cancer, multiple myeloma and potentially other cancers.
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Masuda, Kenta, Megumi Satake, and Daisuke Aoki. "Hereditary Ovarian Cancer." In Hereditary Breast and Ovarian Cancer, 93–106. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-4521-1_7.

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Clarke, Angus. "Breast and ovarian cancer." In Harper's Practical Genetic Counselling, 415–20. Eighth edition | Boca Raton : CRC Press, [2020] | Preceded by Practical genetic counselling / Peter S. Harper. 7th ed. 2010.: CRC Press, 2019. http://dx.doi.org/10.1201/9780367371944-31.

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Miyashita, Minoru, and Takanori Ishida. "Hereditary Breast Cancer." In Hereditary Breast and Ovarian Cancer, 79–92. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-4521-1_6.

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Kobayashi, Hiroshi. "Chemoprevention for Ovarian Cancer." In Hereditary Breast and Ovarian Cancer, 149–67. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-4521-1_10.

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Watanuki, Rurina, Aiko Nagayama, Tetsu Hayashida, and Yuko Kitagawa. "Chemoprevention for Breast Cancer." In Hereditary Breast and Ovarian Cancer, 129–48. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-4521-1_9.

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Black, D. M., and E. Solomon. "The BRCA1 gene in sporadic breast and ovarian cancer." In Ovarian Cancer 3, 39–44. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4757-0136-4_4.

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Lux, Michael P., Mayada R. Bani, Peter A. Fasching, and Matthias W. Beckmann. "Hereditary Breast and Ovarian Cancer." In The Molecular Basis of Human Cancer, 401–21. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-59745-458-2_26.

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Murakami, Wakana, Mitsuhiro Tozaki, Kelly E. McCann, and Stephanie Lee-Felker. "Risk-Based Breast Cancer Screening." In Hereditary Breast and Ovarian Cancer, 107–28. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-4521-1_8.

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Inuzuka, Mayuko. "Genetic Counseling in Hereditary Breast and Ovarian Cancer." In Hereditary Breast and Ovarian Cancer, 65–77. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-4521-1_5.

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Conference papers on the topic "Lung and breast/ovarian cancer":

1

Lemos, Nathalia Oliveira, Fábio Bagnoli, Maria Antonieta Longo Galvão Silva, José Francisco Rinaldi, and Vilmar Marques de Oliveira. "INVASIVE LOBULAR BREAST CANCER METASTATIC TO THE ORBIT: A CASE REPORT." In XXIV Congresso Brasileiro de Mastologia. Mastology, 2022. http://dx.doi.org/10.29289/259453942022v32s1048.

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Invasive lobular carcinoma represents 5%–15% of breast carcinomas, presenting in many cases as multicentric and bilateral tumors with low mammographic detection. The most common breast cancer metastases are the bones, lungs, brain, and liver. However, the disease can also spread to abdominal cavity, ovaries, and skin. The orbit is an infrequent site of tumor metastasis, ranging from 1% to 13% among all orbital tumors, and breast, lung, and prostate are among the most common primary sites. We report the case of a 73-year-old female patient who presented with a palpable mass in the left orbital rim, whose incisional biopsy revealed a pattern compatible with invasive breast carcinoma with lobular characteristics and E-cadherin overexpression, luminal molecular subtype B. She denied breast complaints and palpable nodules, but on clinical examination she showed a tumor in the inferolateral quadrant of the left breast measuring 6 cm and a left axilla with lymph node enlargement suspected of lymph node involvement. Mammography identified suspicious nodulation in this topography, confirmed by ultrasound. The diagnosis made through core biopsy was an invasive breast carcinoma with lobular characteristics, and the immunohistochemical profile showed luminal molecular subtype B. Systemic staging revealed involvement of the retroperitoneum, left ovarian annex, vertebral bodies, pelvis, right femur, and left iliac suspected for secondary involvement. The patient is currently undergoing adjuvant systemic treatment.
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Nguyen, Dat, Larry Rubinstein, Mark E. Sherman, Joseph E. Tomaszewski, Naoko Takebe, Percy Ivy, James H. Doroshow, and Sherry X. Yang. "Abstract 3838: Differential expression of Notch1 in lung, ovarian and breast cancers." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3838.

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GEVAERT, O., S. VAN VOOREN, and B. DE MOOR. "INTEGRATION OF MICROARRAY AND TEXTUAL DATA IMPROVES THE PROGNOSIS PREDICTION OF BREAST, LUNG AND OVARIAN CANCER PATIENTS." In Proceedings of the Pacific Symposium. WORLD SCIENTIFIC, 2007. http://dx.doi.org/10.1142/9789812776136_0028.

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Gansmo, Liv B., Merete Bjørnslett, Anne Dørum, Helga Salvesen, Pål Romundstad, Kristian Hveem, Lars Vatten, Per Eystein Lønning, and Stian Knappskog. "Abstract 4613: MDM4 SNP 34091 (rs4245739) effect on risk of breast, colon, lung, prostate, endometrial and ovarian cancer." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4613.

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Halim, Abdel-baset, Lisa M. Dauffenbach, Christopher A. Kerfoot, William R. Stull, Esther Zwick-Wallasch, Richard Scheyer, and Giorgio Senaldi. "Abstract 3148: Immunohistochemical analysis of HB-EGF expression in breast, colon, gastric, hepatocellular, lung, ovarian, pancreatic and prostate cancer." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3148.

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Fredolini, Claudia, Davide Tamburro, Santosh Goud, Chandler King, Weidong Zhou, Paul Russo, Virginia Espina, et al. "Abstract 4787: Novel upfront sample enrichment nanotechnology identifies prostate, breast, colon, ovarian, lung, pancreatic, and melanoma cancer specific biomarker candidates." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4787.

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Pirie-Shepherd, Steven R., Iman Jilani, Eric Tucker, David Valenta, Ryon Graf, Amanda Anderson, Dena Marrinucci, Puja Sapra, and Eric L. Powell. "Abstract 565: Circulating tumor cell (CTC) detection and 5T4 characterization in breast, ovarian, and lung cancer patients on active therapy." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-565.

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Omofuma, Omonefe O., David P. Turner, Lindsay L. Peterson, Anwar T. Merchant, Jiajia Zhang, and Susan E. Steck. "Abstract C033: Dietary advanced glycation end products (dAGEs) and breast cancer by race in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial (PLCO)." In Abstracts: Twelfth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; September 20-23, 2019; San Francisco, CA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7755.disp19-c033.

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Borges, Isabella Sabião, João Victor Aguiar Moreira, Eustaquio Costa Damasceno Junior, Alencar Pereira dos Santos, Gabriela Tomás Alves, Leonardo Peixoto Garcia, Maria Fernanda Prado Rosa, et al. "Chronic inflammatory demyelinating polyradiculoneuropathy induced by paclitaxel." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.413.

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Background: Peripheral neuropathies in cancer are most often due to neurotoxic chemotherapeutic agents. Approximately 30% of patients receiving neurotoxic chemotherapy (CTX) will suffer from chemotherapy-induced peripheral neuropathy (CIPN). Paclitaxel is an extremely effective chemotherapeutic agent for the treatment of breast, ovarian, and lung cancer. However, paclitaxel-induced peripheral neuropathy occurs in 59-87% of patients who receive this drug. Paclitaxel is an anti-tubulin drug that causes microtubule stabilization, resulting in distal axonal degeneration, secondary demyelination and nerve fiber loss. Case: We present a case of a 68-year-old female patient with history of breast cancer who presented sensorial ataxia and progressive muscle weakness two months after starting CTX with paclitaxel. The physical examination showed tetraparesis with proximal predominance, areflexia, severe hypopalesthesia and postural instability. Electroneuromyography showed the existence of asymmetric demyelinating polyradiculoneuropathy, with conduction block and temporal dispersion in practically all evaluated nerves. The cerebrospinal fluid confirmed the albumin-cytological dissociation. Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) was confirmed and patient underwent monthly treatment with methylprednisolone with good response. Discussion: Evidences has implicated neuroinflammation in the development of PIPN. While most CTX drugs do not cross the blood-brain-barrier, they readily penetrate the blood-nerve-barrier and bind to and accumulate in dorsal root ganglia and peripheral axons. CTX can induce neuroinflammation through activation of immune and immune- like glial cells. In fact, immune cells (e.g., macrophages, lymphocytes) and glial cells (e.g., Schwann cells) in the peripheral nervous system play important role in the induction and maintenance of neuropathy. Conclusion: CIDP should be included in the spectrum of CIPN.
10

Liu, H., and S. Muralitharan. "A Survey of NY-BR-1 Immunohistochemistry in Breast, Ovarian, Endometrial and Lung Cancers: A Correlation Study with Estrogen and Progesterone Receptors." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-6018.

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Reports on the topic "Lung and breast/ovarian cancer":

1

Tennis, Meredith A., and Peter G. Shields. Gene Environment Interactions in Women with Breast Cancer and Secondary Lung Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada428946.

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Tennis, Meredith A., and Peter G. Shields. Gene Environment Interactions in Women With Breast and Secondary Lung Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2005. http://dx.doi.org/10.21236/ada456364.

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Boushey, Carol, Jamy Ard, Lydia Bazzano, Steven Heymsfield, Elizabeth Mayer-Davis, Joan Sabaté, Linda Snetselaar, et al. Dietary Patterns and Breast, Colorectal, Lung, and Prostate Cancer: A Systematic Review. U.S. Department of Agriculture, Food and Nutrition Service, Center for Nutrition Policy and Promotion, Nutrition Evidence Systematic Review, July 2020. http://dx.doi.org/10.52570/nesr.dgac2020.sr0104.

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Frost, Marlene H., Charles Loprinzi, Ann Kearns, Jeff Sloan, and Debra Barton. Changes in Ovarian Stromal Function in Premenopausal Women Undergoing Chemotherapy for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2005. http://dx.doi.org/10.21236/ada446278.

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Barton, Debra, Jeff Sloan, Charles Loprinzi, and Ann Kearns. Changes in Ovarian Stromal Function in Premenopausal Women Undergoing Chemotherapy for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2004. http://dx.doi.org/10.21236/ada428981.

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Goldgar, David E. Identification and Genetic Mapping of Genes for Hereditary Breast Cancer and Ovarian Cancer in Families Unlinked to BRCA1. Fort Belvoir, VA: Defense Technical Information Center, September 1995. http://dx.doi.org/10.21236/ada301314.

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Neuhausen, Susan L. Identification and Genetic Mapping of Genes for Hereditary Breast Cancer and Ovarian Cancer in Families Unlinked to BRCA1. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada382834.

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Frost, Marlene H. Changes in Ovarian Stromal Function and Associated Symptoms in Premenopausal Women Undergoing Chemotherapy for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2008. http://dx.doi.org/10.21236/ada510068.

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9

Wang, Yan, Wenpeng Song, Sicheng Zhou, Jie Tian, Yingxian Dong, Jue Li, Junke Chang, et al. Increased risk for subsequent primary lung cancer among female hormone-related cancer patients: a meta-analysis based on over four million cases. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2022. http://dx.doi.org/10.37766/inplasy2022.7.0044.

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Review question / Objective: To identify the risk of lung cancer in FHRC patients compared to the general population. Condition being studied: The incidence rate of lung cancer in women is obviously increasing over the past decade and previous evidence have indicated the significant relationship between disturbances in hormone levels and the risk of lung cancer. Therefore, we hypothesized female hormone-related cancer (FHRC), including the breast, endometrial, cervix, and ovary cancer, patients may experience a higher risk of developing subsequent lung cancer.
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Battaglia, Tracy, Christine Gunn, Sharon Bak, JoHanna Flacks, Kerrie Nelson, Na Wang, Naomi Ko, and Samantha Morton. Reducing Legal Barriers to Help Patients Receive Treatment for Breast and Lung Cancer—The Project SUPPORT Study. Patient-Centered Outcomes Research Institute (PCORI), July 2020. http://dx.doi.org/10.25302/07.2020.ad.13046272.

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